Commentary: Considerations for the IR Horse

Eleanor Kellon, VMD, staff veterinary specialist for Uckele Health & Nutrition, shares her thoughts on the state of insulin resistance in horses. (Editor's Note: If you believe your horse is IR, work with your veterinarian to develop a management plan designed to best treat each specific animal.)

Equine insulin resistance (IR) has been so well publicized everyone has heard of it. However, few really understand what it is, what causes it, and what to do about it.

Parallels have been drawn between equine insulin resistance/metabolic syndrome and human type 2 diabetes. While some of them are indeed valid, others are not and this complicates efforts to treat the horses correctly.

There is nothing new about IR. What's new is that we recognize it for what it is. The stereotype of an overweight pony as high risk for pasture laminitis is timeless. The existence of laminitis prone lines in horse breeds, such as Arabians and Morgans, has been more of a secret. Some lesser known breeds, like Peruvian Pasos, are highly prone to IR but their breeders and aficianados are very aware of their propensity.

Between 1975 and 2002, when Philip Johnson (BVSc (Hons), MS, Dipl. ACVIM, Dipl. ECEIM, MRCVS) published his first paper using the term equine metabolic syndrome, there were three papers published linking IR and laminitis. These did not make mainstream veterinary medicine, let alone veterinary school curricula. In 1999, I did a field trial of magnesium supplementation for cresty laminitic horses/ponies based on a "folk remedy" in the U.K. Surprisingly, it actually helped. A literature search revealed a strong link between magnesium deficiency and IR in humans and ultimately those early equine studies.

Dr. Johnson's 2002 paper brought equine IR to the forefront, but there was considerable resistance to the idea that insulin resistance not related to Cushing's disease (high cortisol in Cushing's disease causes IR) even existed. One of the most vocal early critics was David Kronfeld (PhD, DSc, MVSc, MRCVS, Dipl. ACVN, Dipl. ACVIM) from the Virginia Polytechnic Institute, but a 2006 study by his group resulted in a complete reversal of his opinion, as it described IR and equine metabolic syndrome as the link to laminitis in a large pony herd maintained on pasture. Review of pedigrees also strongly pointed to a genetic component, which is compatible with the observation that IR tends to affect some breeds and not others. From that point forward 5 years ago, recognition of the significance of IRF among practicing veterinarians and in veterinary schools has sky rocketed.

Today, IR is the disease du jour. As is often the case with high profile disorders, it is now being overdiagnosed without proper testing. Obesity, a host of hoof ailments/abnormalities, even thrush, is being blamed on IRF. As a result, many horses are being placed on very restrictive diets that should not be, and the real cause of their problems is not being addressed.

One outgrowth of the rush to blame IR for everything is that every overweight horse is being labeled as insulin resistant. However, a large field study done by the Maryland Virginia Regional College of Veterinary Medicine found that only 35% of even very obese horses are actually insulin resistant. The prevalence of IR across all weights and breeds is about 10 to 15%. With an estimated equine population in this country of about 10 million horses, this is still a very considerable number.

Diagnosis by symptoms is simply not reliable. Fortunately, blood work usually clearly differentiates between normal and insulin resistant horses. You need a serum insulin and glucose taken after 12+ hours of nothing to eat except hay or pasture. No fasting. Hay or pasture available all the time. This protocol comes from the Virginia Polytechnic pony field study. Results can then be uploaded to the IR calculator for interpretation.

The most recently available test is one that detects serum leptin and is available from Cornell University's diagnostic laboratory. Leptin is a hormone released by fat cells which in normal horses turns off appetite. However, IR horses are leptin resistant and have elevated levels of this hormone.

Insulin's job is to trigger the uptake of glucose from the blood into tissues that are dependent on insulin for this function, including fat, skeletal muscle, and liver. With IR, the insulin sensitive tissues do not respond to normal levels of the hormone. As a result, the pancreas increases output of insulin in an attempt to normalize blood sugar.

Experiments using infusions of either insulin or glucose in normal horses and ponies have established that the laminitis associated with IR is caused by high insulin, not high glucose. Horses with IR rarely are actually diabetic. Diabetes mellitus by definition is elevated blood sugar.

In humans, insulin resistance in the liver results in high blood glucose. The liver can produce glucose when blood glucose drops (e.g. overnight or between meals), and shuts off this production as insulin rises in response to the glucose. With IR in the liver, the insulin signal is not read correctly and glucose production continues.

This is why, even with fasting, a human with IR/type II diabetes will have elevated blood glucose (and insulin). On the other hand, fasting a horse with IR can lead to a false negative test, with insulin and glucose appearing normal.

Because of liver insulin resistance in people, the focus of therapy, whether pharmaceutical or alternative/herbal, is primarily on lowering blood glucose, often by agents that increase the production of insulin. There are also agents like chromium or cinnamon that mimic the action of insulin. Agents that cause higher insulin may actually increase laminitis risk, while those that work like insulin and lower glucose lead to drops in glucose but no change in insulin level.

The most successful therapy for IR in both humans and horses is exercise and diet control. Exercise primes the muscle to take up glucose by pathways that are independent of insulin, resulting in less work for insulin to do and improved IR. The effect lasts for about 24 hours.

On the diet front, avoiding blood sugar spikes avoids insulin spikes. What constitutes a "low" carbohydrate diet is very different for humans versus horses. A horse eating nothing but pasture will likely never encounter a combined simple sugar and starch level over 15%. Couple this with moving an average of 20 miles per day and the feral horse does not have a problem.

However very few domesticated horses cover 20 miles per day. Without the protective exercise, susceptible horses are primed to develop problems with IR if their diet is not carefully restricted. Most IR horses need a hay based diet with combined simple sugars (ethanol-soluble carbohydrates, or ESC, on hay analysis) and starch of 10% or lower.

Feeding fat does not cause an insulin spike. Normal horses fed diets with concentrates high in fat and fiber versus grains will be more insulin sensitive. The natural diet, grass, contains 4 to 6% fat. Omega-3 fatty acids comprise 50% of the fat in grass and are the most fragile, rapidly lost with curing. Since many IR horses are on hay with no pasture access, it is important to replace the lost essential fatty acids.

Flax seed is an excellent source of omega-3, as it has an omega-3:omega-6 ratio that mimics fresh grass. Small amounts of oil (up to 1 oz/500 pounds body weight) can also be used, to enhance vitamin E absorption and prevent dust from added supplements. A particularly good source of oil is unrefined, so contains natural vitamin E and tocotrienols, is lower in omega-6 and highly palatable.

So what does work for insulin resistant horses?

Diet of hay or hay and beet pulp, with ESC (i.e., simple sugars) plus starch content no higher than 10%;

Added flax seed to supply essential fatty acids in a ratio that approximates the naturally found level in grasses;

Balanced minerals, preferably based on a hay analysis, with generous magnesium (calcium:magnesium ratio no higher than 2:1) and careful balancing of trace minerals, with supplemental salt and vitamin E; and

When possible, exercise, exercise, exercise!

On the drug front, there are multiple options for people but the only one that actually improves insulin sensitivity is metformin. Metformin has also been studied in horses and while results are somewhat contradictory is does appear to be a good choice for getting rapid control of IR, at least for a few weeks, while other measures can be put into place.

Most herbals used for human type II diabetes are not appropriate for horses because they raise insulin without really addressing IR. One exception is North American Ginseng, Panax quinquefolius, which can actually increase insulin sensitivity in other species. Gynostemma pentaphyllum (Jiaogulan) also has insulin sensitizing effects in studies from multiple species and is helpful in supporting circulation in laminitic horses.

Acetyl-L-carnitine is a naturally occuring metabolite that influences a "master switch" enzyme in the cells causing increased glucose utilization and improved glycogen levels. Glycogen is a storage form of glucose that is typically low in insulin resistance. This metabolite is also helpful for neurogenic pain (which results from alterations in nerves in situations of chronic pain). It has been very helpful for some horses with chronic laminitis pain. As a side bonus, abnormal fatty deposits typical of IR, like fatty neck crests, improve slowly with acetyl-L-carnitine supplementation.

Insulin resistance in horses is not so much a "disease" as it is a metabolic type that requires a specific management and diet. Insulin resistance allows horses to gain weight easily and hold their weight better under conditions of sparse food supply. Its roots are almost certainly genetic. However, what worked for ancestors struggling to find food does not work under domestication.

There are no magic bullets and no short cuts with IR. Exercise is often the missing element with domestic horses and matching the ancestral exercise level is difficult if not impossible for most people. This necessitates tighter control of sugar and starch in the diet of horses prone to IR. While this may seem like more trouble on the surface, it's really not and the IR prone horse is much less expensive to keep on the bottom line.

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